The present invention generally relates to an implantable cardiac stimulation device. The present invention more particularly relates to such a device and a method for treating an accelerated junctional rhythms, accelerated idioventricular rhythms, and marked first degree AV block, all of which may result in inhibition of a dual-chamber pacemaker leading to symptoms associated with the loss of appropriate atrioventricular synchrony and its associated atrial contribution to ventricular filling.
Implantable cardiac stimulation devices are well known in the art. They include implantable pacemakers which provide stimulation pulses to a heart to cause a heart, which would normally or otherwise beat too slowly or at an irregular rate, to beat at a controlled normal rate. They also include defibrillators which detect when the atria and/or the ventricles of the heart are in fibrillation and apply cardioverting or defibrillating electrical energy to the heart to restore the heart to a normal rhythm. Implantable cardiac stimulation devices may also include the combined functionalities of a pacemaker and a defibrillator.
As is well known, implantable cardiac stimulation devices sense cardiac activity for monitoring the cardiac condition of the patient in which the device is implanted. By sensing the cardiac activity of the patient, the device is able to provide cardiac stimulation therapy when it is required.
In a healthy heart, the sinoatrial node (SA node) serves as the natural pacemaker of the heart. It is a group of specialized myocardial cells located on the posterior wall of the upper right atrium at the junction between the atrium and the superior vena cava. It initiates electrical impulses in the heart""s myocardium at a more rapid rate than other myocardial cells.
The atrioventricular node (AV node) transmits electrical signals from the atria to the ventricles. It is a small concentration of specialized conductive tissue at the base of the atrial septum. The AV node serves an important role in maintaining atrioventricular synchrony, the sequence of an atrial depolarization followed by a ventricular depolarization after an appropriate PR interval. Maintenance of atrioventricular synchrony enhances cardiac output and the loss of it (loss of atrial transport) may reduce cardiac output by 10 to 30%. If the SA node fails, the AV node is capable of serving as a back-up pacemaker of the heart. However, the cardiac rate, under such circumstances, is generally lower than normal (40 to 60 beats per minute) and without atrial transport. However, in special circumstances, the junctional pacemaker may accelerate and usurp control from an otherwise normal sinus node. In the setting of sinus node dysfunction for which a pacemaker was implanted, the junctional focus may accelerate and usurp control from the otherwise normal dual-chamber pacemaker.
Accelerated junctional rhythms may occur as a consequence of AV nodal ablation, intrinsic disease involving the atrioventricular node or junction, as a consequence of metabolic imbalance or as a side effect of a multiplicity of medications.
Hence, patients with SA node dysfunction or who have had their AV node ablated generally have a demand pacemaker to regulate their heart rhythm. While such devices do regulate cardiac rhythm, these patients can experience accelerated junctional rhythms. These rhythms occur at a relatively high rate as a result of parasympathetic withdrawal or increased sympathetic stimulation. The intrinsic rhythm will be sensed by the pacemaker causing it to inhibit. The result is a loss of atrial transport. This abnormal rhythm may be associated with retrograde conduction to the atrium. In both circumstances, hemodynamics and cardiac output may be compromised. Also, under these conditions, the implanted demand pacemakers may be unable to provide assistance as the high rate may cause these devices to be inhibited.
A similar rhythm, but arising from a ventricular focus, is termed accelerated idioventricular rhythm (AIVR). It will have similar consequences with respect to compromising hemodynamics and for the patient who has a dual-chamber pacemaker, result in its inhibition. This rhythm may be associated with retrograde conduction.
A third rhythm is a sinus rhythm with marked first-degree AV block. At accelerated rates, the sinus P wave is appropriately tracked. However, in the setting of either an atrial premature beat that occurs so early as to coincide with the portion of the pacemaker""s timing cycle where the atrial channel is refractory or a ventricular premature beat initiating a PVARP with the sinus beat thus coinciding with this refractory period, the P wave will not be tracked. However, if AV nodal conduction is intact, but with very slow conduction (a long time required to conduct from the atrium to the ventricle), the resulting native ventricular depolarization will cause the pacemaker to be inhibited. The result is that appropriate AV synchrony will be lost and the pacemaker will be inhibited.
In each of these three rhythms, there is an intrinsic ventricular rhythm effectively inhibiting the pacemaker yet each is associated with the loss of an optimal AV delay compromising cardiac function.
The present invention provides an implantable dual-chamber cardiac device and method for treating intrinsic ventricular rhythms lacking in atrial transport. A rhythm detector detects an intrinsic ventricular rhythm lacking in atrial transport when an R-wave detector detects a predetermined number of successive R-waves at a rate below a given rate and when each successive R-wave fails to be preceded by an atrial event, either intrinsic or paced.
When this rhythm is detected, an atrial pulse generator delivers an atrial pacing pulse to an atrium of the heart prior to each successive R-wave. The atrial pacing pulses are delivered an AV delay prior to the R-waves and the pacing rate is held constant for a time period. Thereafter, the pacing rate is gradually reduced during a recovery time period until a base rate is reached or until the end of the recovery time period.
If the period of AR pacing is supplanted by another intrinsic ventricular rhythm lacking in atrial transport, the device again begins delivering atrial output pulses at an appropriate time prior to the R-waves.
An intrinsic ventricular rhythm lacking atrial transport may also be detected by detecting successive R-waves succeeded by corresponding P-waves occurring during corresponding relative post-ventricular atrial refractory period intervals. When such a rhythm is detected, a pacing pulse is applied to an atrium a time period after each refractory sensed P-wave. The time period is selected to be sufficiently long to enable full recovery of the atria to render the pacing pulses effective in capturing the atria and restoring AV synchrony.
In accordance with the present invention, atrial transport is restored when the pulse generator would otherwise be inhibited. Further, the heart rate is returned to a more normal rate.
The device and method may further be used to treat intrinsic ventricular rhythms lacking atrial transport including accelerated junctional rhythms, accelerated idioventricular rhythms as well as marked first degree AV block that results in inhibition of a dual or multichamber pacing system. The present invention may be used to advantage in a stand-alone implantable dual-chamber pacemaker or in an implantable device having both a dual-chamber pacemaker and a cardioverter/defibrillator.